Collapsing Trachea

The trachea, also known as the windpipe, is an important structure which connects the throat to the lungs. It is composed of 35- 45 C-shaped rings of cartilage that are joined by muscle and ligaments to create a tube-like structure. It serves the purpose of directing air into the respiratory tract.

When the cartilage rings are flattened from the top to the bottom, the trachea is said to be collapsed. Rapid inhalation of air can cause the trachea to flatten and make it difficult for air to enter the lungs, much like a soda straw being drawn on too vigorously.

Why does it happen?

We do not completely understand how this condition develops. However, we know that these dogs have an abnormality in the chemical makeup of their tracheal rings. The rings loose their stiffness so they are not able to retain their circular shape. We also know that it occurs in certain breeds of dogs, notably Chihuahuas, Pomeranians, Shih Tzus, Lhasa Apsos, Toy Poodles, and Yorkshire Terriers. Because of that, it is suspected that there is a genetic factor involved.

What are the signs?
Collapsing trachea or Reverse sneezing

With reverse sneezing the pharynx (back of the throat) goes into spasms. The dog finds it difficult to draw in air through the spasms, so it stands still, stretches out her neck, and thrusts its elbows out (like a bowlegged bulldog) as it honks, wheezes, or snorts. Often eyes open wide. The spasms will stop if she swallows a couple of times.

•Close off her nostrils with your fingers so it has to breathe through its mouth for a few seconds.
•Gently rub its throat. This works for some.
•Distract it by carrying the dog outside into the fresh air.

Young puppies can reverse sneeze, but the first episode typically occurs in late adolescence. Stay calm and get it to swallow with one of the methods described above. In a few seconds to a minute, it will run off to play. Reverse sneezing is a harmless phenomenon which needs no vet consultation and no medical treatment whatsoever. It is very common in toy breeds.

Other signs, however, will help you distinguish the two conditions:
If it makes these sounds when excited or after eating or drinking, or turns her elbows outward and extends its neck and gasps inward with a rhythmic snork! snork! snork!, this is reverse sneezing.
If it breathes through the mouth sometimes, or breathes with a raspy sound, or coughs reflexively when you simply rub its throat, it could have a collapsing trachea. If the cough is one or two expulsive outward bursts (forcing air through the trachea to open it), typically with a gag or empty retch at the end, she could have a collapsing trachea.

The most common clinical sign of collapsing trachea is a chronic cough. It is often described as dry and harsh and can become quite pronounced. The term "goose honk" is often used to describe it. Coughing is often worse in the daytime and much less at night. The cough may also begin due to excitement, pressure on the trachea (from a leash), or from drinking water or eating.

How is collapsed trachea diagnosed?

Many times, very light pressure placed on the trachea during the physical examination can raise a suspicion of collapsed trachea in a small dog with a persistent dry cough. While the information gained from the physical examination is helpful, other tests are needed to confirm this condition.
X-rays of the chest can identify the trachea and its shape. However, a collapsed trachea changes its diameter during the respiratory cycle. It is usually collapsed during inhalation and normal during exhalation. Therefore, attempts to make radiographs during both phases of respiration should be made.
Endoscopy is another way to see the trachea. An endoscope is a tube that is small enough to be inserted into the trachea. By watching the trachea during inspiration and expiration, abnormal collapsing can be seen. Unfortunately, tracheal endoscopes are expensive and not available at every veterinary hospital.

How is it treated?

Collapsed trachea can be treated medically or surgically. Some dogs respond well to:

• bronchodilators and various types of anti-inflammatory drugs.
•chemical cough suppressants
•a bronchodilator (typically the drug aminophylline) to keep the bronchial tubes open in extreme cases that are affecting the lungs
•The trachea of these dogs is easily infected, so antibiotics are usually part of the treatment.
•If obesity is present, weight loss is often beneficial.
•Excitement and vigorous exercise are likely to cause a relapse, so they should be avoided as much as possible.

Because medical therapy only treats the symptoms and not the problem, these dogs are always subject to recurrences of coughing and breathing difficulty.

•Surgery. The above tests are used to determine how much of the trachea is collapsed. If the only abnormal part is that segment between the throat and the point where the trachea enters the chest (the thoracic inlet), surgery may be curative. However, if the segment of the trachea that is within the chest cavity is abnormal, surgery is not likely to be helpful because that part is not accessible to the surgeon. There are several surgical approaches that have been used. Each approach implants an artificial support device that is secured around or within the trachea. The purpose of the support device is to hold the tracheal rings in their normal, open position. Although some dogs have excellent results and are truly cured of the disease, the outcome is not uniformly successful.

Natural ways to treat your Yorkie:

•Fresh foods, keeping the amounts low for weight reduction. Fat dogs have a much harder time breathing.
•Vitamin C
•Vitamin E
•Exercise reduction. Don't stop exercise completely -- just don't let get to the point where the dog is panting heavily, especially when older. Remove all pressure from the throat. No collars, and use a harness that wraps around the chest and stomach, never around the throat. Tell visitors not to rub the throat.
•A cool-mist humidifier to keep the air moist and easy to breathe.
•Glyco-flex and Glucosamine are nutritional products packed with minerals, amino acids, enzymes, and lubricating agents. They build cartilage and help heal damaged connective tissue. These are natural products with no side effects. They are inexpensive and last a very long time, so you have absolutely nothing to lose by trying them.
•Herbal cough remedies, if coughing is really bad.

For more information visit Mary Kay Keppler's article on collapsing trachea

•Animal Clinic Collapsing trachea in the dog Retrieved February 1998 from the WWW
•Potter, Clayton Dr. Heartland Veterinary Hospital Retrieved February 1998 from the WWW
•Chihuahua Kingdom Retrieved February 1998 from the WWW
•Richard, Michael, DVM Q&A-Dr Mike Retrieved February 1998 from the WWW
•Seranne, Ann (1980) The Joy of Breeding Your Own Show Dog New York Macmillian Publishing Company.

Liver Shunt

This condition is often referred to as a "liver shunt" but the current favored term appears to be portosystemic shunt. These have also been referred to by more exact terms since there are specific types of shunts that vary slightly. The broad categories are extrahepatic and intrahepatic shunts, depending on whether or not the shunt occurs in the liver or outside of it. Specific types of shunts are patent ductus venosus, portal-azygous, portocaval (portal-abdominal vena cava), atresia (lack of development) of the portal vein and acquired shunts that occur due to
changes in blood pressure or circulation.

Yorkshire terriers are reported to have a higher than normal incidence of liver shunts. They are reported to be more likely to have extra-hepatic shunts which is good since they are easier to repair.

What are the signs?
Most shunts cause recognizable clinical signs by the time a dog is a young adult but once in a while one is diagnosed at a later time in life. Since the severity of the condition can vary widely depending on how much blood flow is diverted past the liver it is possible for a lot of variation in clinical signs and time of onset of signs to occur. Often, this condition is recognized after a puppy fails to grow, making an early diagnosis pretty common, too.
Signs of portosystemic shunts include poor weight gain, sensitivity to sedatives (especially diazepam), depression, head pressing (pushing the head against a solid object), seizures, weakness, salivation, vomiting, poor appetite, increased drinking and urinating, balance problems and frequent urinary tract disease or early onset of bladder stones. If the signs of problems increase dramatically after eating this is a strong supportive sign of a portosystemic shunt.

How is Liver Shunt diagnosed?
This is frustrating since there is not a test for this condition. There was a "definitive" test and there is almost one - special dyes injected into the liver circulation that show up on X-rays can outline the problem pretty clearly. Most of the time. But this is a pretty invasive test making it a poor choice for "screening" purposes. There are a number of possible abnormalities that might point towards a portosystemic shunt on routine labwork, including low BUN (blood urea nitrogen), low albumin, mild anemia, increases in ALT (serum alanine aminotransferase) or ALKP (serum alkaline phosphatase). If these hints are present, it would be a good idea to test the serum bile acid levels prior to eating and after eating. If this test is supportive of poor liver function then it may be a good idea to consider ultrasonagraphy and dye contrast X-rays.

How is it treated?

So far in my research I haven't found a cure for Liver shunt besides surgery for portosystemic shunts. As far as I know, dogs with extrahepatic shunts (occurring outside the liver itself) is easier to do than surgery in dogs with intrahepatic (inside the liver) shunts. If you know of a different cure please let me know.

by Larry Snyder, DVM

Clinical Signs: Most dogs will be diagnosed with port-systemic shunts under one year of age, but dogs as old as eight have been diagnosed with the condition. Animals are usually stunted, thin, depressed, have trouble gaining weight, and are usually characterized by the owners as chronic "poor doers". In most affected dogs there will be some degree of behavioral signs ranging from listlessness, apathy, or depression to more severe signs of circling, head pressing, stupor, drooling, blindness, or convulsions, some leading to coma. These behavioral changes are due to an accumulation of toxins (especially ammonia) that affect the brain causing a condition called Hepatic Encephalopathy. These toxins are most abundant in the blood stream following the dog eating, especially a high protein meal, & may remain high for hours afterward. Not all dogs with the shunt will show this meal associated behavioral change, but in 25% of the affected dogs that do, the diagnosis becomes clearer. A high percent of affected animals show an intolerance to anesthetics or tranquilizers, & will show increased recovery times following use of these products. Even anti-convulsants used to control seizures may be potentially dangerous if allowed to concentrate in a dog with functional shunt. Approximately 75% of affected individuals will show digestive system symptoms including poor appetite, ascites, vomiting, drooling, diarrhea, or occasionally deranged appetite (eating paper, etc.). Urinary system symptoms may include increased thirst and urination, & in a majority of porto-systemic shunt cases, there will be crystals or stones formed in the urinary tract. These crystals will be either uric acid or ammonium urate (ammonium biurate or thorn-apple crystals.). There can be bladder stones formed or crystals may be noted on the hair around the prepuce or vulva.

Laboratory Findings: Routine performed serum chemistries are fairly nonspecific toward confirming the diagnosis of porto-systemic shunts, but there may be a decreased total protein (primarily albumin), decreased blood glucose, decreased cholesterol, & decreased blood urea nitrogen (BUN). The uric acid levels may be elevated in a significant number of affected individuals. Acid levels are extremely important in the diagnostic screening of symptomatic potential shunts. Fasting and 2-hr. post meal blood samples are evaluated for bile acid levels. In virtually all porto-systemic shunts there will be a significant rise in the bile acid levels over normal. The use of bile acids in screening clinically normal dogs for liver shunts is not currently being advised due to the variation of normal bile acid levels in Yorkshire Terriers, & other breeds as well. Reports of recent vaccination with modified-live vaccines causing high serum bile acid levels in normal animals have not been confirmed as of this time. Liver function testing with Bromosulfaphthalein (BSP) or ammonia tolerance testing are sensitive & reliable if performed correctly. These tests measure the liver's ability to excrete/detoxify known agents, and thus measure liver function accurately.

Radiography. Radiography is one of the most important methods of establishing a diagnosis of porto-systemic shunt, & is currently the only universally accepted method of confirming a shunt, short of major surgery. Injection of a radiopaque dye into the spleen (Splenoportograpy) will show the shunt on radiographs & allow accurate assessment for surgical correction.

Nuclear Medicine. The placement of a radiopharmaceutical agent (radioisotope) specific for the liver into the colon for absorption through the mucosa has been gaining favor because of its noninvasive diagnostic value. This procedure requires expensive equipment & the diagnosis is based on the distribution of the radionuclide in the lung or heart compared to that in the liver. This procedure also does not identify the exact location of the shunt for surgical correction if required.

Ultrasound. Until recently, ultrasound was fairly unreliable for nonsurgical diagnosis of porto-systemic shunts. With the advent of Color Flow Ultrasound, there is the potential for diagnosis of this condition on non-anesthetized animals. At the present time, this technology appears to be the diagnostic procedure of choice. If currently undertaken research confirms its value, Color Doppler Ultrasound will soon be the preferred screening and diagnostic tool.

At the present time, Hepatic Porto-Systemic shunts are considered to be UNQUESTIONABLY genetic by some of the leading canine experts, but the mode has not been identified at the present time; research is being conducted at Michigan State University to identify this pattern. Genetic disorders in dogs can spread relatively rapidly if a dog, whether affected or a carrier, is a well-respected animal in either conformation or ability, and is used extensively for breeding. This is especially true in the case of the male that can produce hundreds of offspring during his breeding life. If the cause of such a condition can be discovered, then a working strategy can be implemented to control and eliminate the disorder.

The Yorkshire Terrier Club of America Foundation, Inc. is currently funding research into both the genetic nature of the problem & into the use of Color Flow Doppler Ultrasound as a diagnostic & screening tool. These steps will hopefully become the basis for setting up an open registry for Yorkshire Terriers & other affected breeds to hopefully eliminate, or at least minimize the problem within each breed.

For More information contact the YTCA

•Richard, Michael, DVM Q&A-DR Mike Retrieved February 1998 from the WWW
•Shumsky, Terri (1993) How to buy your Toy Dog, and Raise it Expensively California Creations by Terri.
•Snyder, Larry D.V.M. YTCA Foundation

(experts from a letter I received 2-10-00) My name is Karen Tobias and I am a surgeon at University of Tennessee College of Veterinary Medicine. I have been studying and surgically correcting portosystemic shunts for 15 years. I have recently received funding from the AKC Canine Health Foundation and the YTCA to study genetics of normal Yorkies and Yorkies with liver shunts.

The Canine Health Foundation of the American Kennel Club and the Yorkshire Terrier Club of America have joined forces to investigate the cause of one of the breed's most heartbreaking diseases: Congenital Portosystemic Shunts. Portosystemic shunts, or "PSS", are abnormal blood vessels that form a bypass around the liver. Toxic blood that is normally filtered and cleansed by the liver is shunted to the heart and brain, resulting in depression, behavior changes, poor growth rate, and other signs of illness in affected dogs.

One out of every seven Yorkshire Terriers presented to Washington State University College of Veterinary Medicine for any reason was found to have a portosystemic liver shunt! The hereditary nature of this birth defect has already been established in Irish Wolfhounds, Maltese, and other breeds. Many breeders assume the disease is genetic in Yorkshire Terriers as well; however, this has yet to be proven.

Goals of our study: Our study will serve as the first step in identifying a genetic cause for Congenital Portosystemic Shunts. By evaluating pedigrees of affected and unaffected Yorkshire Terriers we will try to answer the following questions: Are liver shunts genetic? Do liver shunts occur equally throughout the breed or is there an increased risk of portosystemic shunts with certain ancestors? What is the risk of inheriting a portosystemic shunt? And, is it likely that we will be able to isolate a carrier gene? If a genetic basis for PSS is found, the information gained can then be used to pursue genetic testing for the condition.

Dr. Karen Tobias can be reach at : Dr. Karen Tobias, Department of Small Animal Clinical Sciences, PO Box 1071, Knoxville TN, 37901-1071.

Luxating Patellas

Luxating is a fancy word for dislocating. Patella is your dog's "knee", the joint on the front of her hind leg. So a luxating patella is a dislocating knee or trick knee, a knee that keeps slipping out of its socket. This can happen in yorkies with weak ligaments, tendons, and/or muscles. It can also happen in Yorkies whose kneecap groove is too narrow or shallow. The knee usually slips inwardly, toward her body, and locks so that your Yorkie can't bend her leg.
Suspect luxating patella if your Yorkie sometimes lifts one hind leg while she is running, or if she often moves both rear legs at the same time, like a hopping bunny.
Sometimes the knee slips only for a few moments, then slides back into place. Sometimes the knee slips out and stays out, and your Yorkie will hold her leg off the ground and limp, perhaps tucking her thigh into her body. Luxation may occur in one knee, or in both. It is seen in many other toy breeds, and in both sexes, though it seems to be more common in females. No matter how firm the knees seem as puppies, toy dogs are liable to injure their knees.

Is luxation serious?
There are four degrees (grades) of luxation:

I. The knee only slips out when the vet manipulates it.
II. The knee luxates occasionally when your Yorkie is walking or running. She may not seem to mind much, or she may shriek, but it usually slides back by itself as she continues moving. Or you can slip it back manually (ask the vet to show you how).
III. The knee luxates frequently and causes chronic lameness. Even when you put it back manually, it doesn't seem to last long.
IV. The knee luxates, stays that way, and you can't put it back into its socket. This grade is very rare.

How is luxation treated?

•The first treatment should be to crated for a week or two and supervise the activity - no jumping.
•Non-steroidal anti-inflammatories (like Rimadyl). These will hide the symptoms, but do absolutely nothing to strengthen or correct the knee.
•Steroidal anti-inflammatories. These are extremely damaging to the immune system, have awful side effects (short and long term), and should never be used.
•Surgery. Surgery is seldom the answer and should only be done by an orthopedic surgeon. Call the American College of Veterinary Surgeons at (301) 718-6504 and ask for a referral to an orthopedic specialist or college of veterinary medicine in your state. If surgery is your choice, that dog will have problems down the road with arthritis from the surgery. In the opinion of most vets, surgery is overkill for Grade I or II luxating patella. I would only go with surgery on a Grade IV luxation, or on a Grade III that did not respond to natural treatment. Surgery costs about five hundred dollars per leg, it is uncomfortable for your Yorkie, and there is a 50% chance that some degree of luxation will return.

Natural ways to treat your Yorkie:

•Feed fresh foods.
•Keep your Yorkie lean. Fat dogs have to carry more weight on their weak leg joint.
•Moderate exercise, walking up slight inclines (gentle hills), will strengthen the muscle groups around the patella.
•Vitamin C is one of the building blocks of strong ligaments and connective tissue.
Glyco-flex and Glucosamine are nutritional products packed with minerals, amino acids, enzymes, and lubricating agents. They build cartilage and cushioning fluid in injured joints, and help heal damaged connective tissue.

What causes luxating patella?

Occasionally it's caused by an injury, but in the absence of such proof, the weak tendons and/or shallow kneecap groove of luxating patella is considered hereditary. Never breed a Yorkie with any degree of luxation (even a "wiggly" knee), whether it has been repaired or not. Fixing the knee doesn't fix the genes that caused the problem.

OFA Certification
The Orthopedic Foundation of America will issue registration numbers to dogs whose patellas have been x-rayed by a vet, forwarded to the OFA, and found to be normal. This condition is so common in Yorkies that we believe it is essential that all breeders start doing these x-rays before breeding. Then you will be able to INSIST on seeing the OFA certificate for each parent before buying a Yorkie puppy. It will be one more way to pick out the responsible breeders from the rest of the pack.

For More Information visit the Orthopedic Foundation of America

•Chihuahua Kingdom Retrieved February 1998 from the WWW
•Shumsky, Terri (1993) How to buy your Toy Dog, and Raise it Expensively California Creations by Terri.

L'egg Perthes

Legg-Perthes, also called Legg-Calve-Perthes (LCP) disease, is a disease of the hip joints of small breeds of dogs. The head of the femur (the ball part of the ball and socket) begins to die and disintegrate. This causes limping, pain, and eventually arthritis. It usually appears between 6-12 months of age. It is treated surgically by removing the head of the femur and letting the muscles form a "false joint." It really does work. The dogs recuperate very well from surgery.

Legg-Calve-Perthes Disease (aseptic or a vascular necrosis of the femoral head)
Avascular necrosis occurs when the bone that makes up the ball portion of the hip is damaged from lack of blood supply. The reasons this occurs are not clear. Since a higher incidence of this disorder is noted in several dog breeds, including terrier breeds, miniature pinscher, poodles and possibly schipperkes, it is assumed that there may be a genetic component to the problem. In Manchester terriers, the genetic component appears to be a strong influence and heritability is pretty high for this problem.
Most of the time the clinical signs of this disease occur in 4 to 11 month old dogs and usually consist of lameness of one leg only. Pain may be mild to very severe. Some dogs have mild forms of this condition and do not require medical care. In other dogs, the condition cause sufficient pain and deformity of the hip joint to require surgical intervention. The disorder can usually be confirmed with X-rays. Atrophy of the muscles of the affected leg is not uncommon. If this is severe it can slow the recovery period considerably and may make medical therapy less likely to work.
Treatment of this condition varies according to the severity of the signs seen. In mild cases, enforced rest may be sufficient to allow healing of the damaged areas to occur. In some cases, immobilization of the affected limb using an Ehmer sling may be beneficial to recovery. Many dogs have advanced cases of this disease by the time they are examined by a veterinarian and medical treatment is not likely to work. In these dogs, excision of the femoral head (ball portion of the hip joint) is often beneficial. Removal of this section of the bone diminishes painful bony contact in the hip joint. Recovery from this surgery can be slow with recovery periods of up to one year sometimes occurring before good use of the affected leg returns. If muscle atrophy is not present at the time of surgery the recovery time is usually much less. Pain relief and anti-inflammatory medications may be beneficial.
There is a stronger tendency to treat this as a medical condition prior to surgery right now. A general rule of thumb is to allow non-surgical therapy a month to show a beneficial response. If one is not seen, surgical repair should be considered more carefully.

•Jack Russel Terrier L'egg Perthes Retrieved February 1998 from the WWW
•Shumsky, Terri (1993) How to buy your Toy Dog, and Raise it Expensively California Creations by Terri.
•Richard, Michael, DVM Q&A-DR Mike Retrieved February 1998 from the WWW http


Eclampsia is an acute, life-threatening disease caused by low calcium levels (hypocalcemia) in dogs and more rarely in cats. The lactating animal is especially susceptible to blood calcium depletion because of lactating. The bodies of some lactating dogs and cats simply cannot keep up with the increased demands for this mineral that they receive from their diet. Please remember that the diet may be fine for these affected individuals, but they lack the ability to quickly shunt calcium to their milk without depleting their own bodies.

Eclampsia is most commonly encountered 1-3 weeks after giving birth, but it can occur anytime, even while pregnant. Litters do not need to be large to cause eclampsia but usually heavy milkers are at a greater risk, as are dogs of smaller breeds. The puppies and kittens themselves are not affected as the mother’s milk appears to be normal during this period.

Signs of eclampsia
Eclampsia is a very serious disorder but fortunately the signs are fairly easy to recognize, especially when coupled with the period of lactation. Initially, the affected animal will be restless and nervous. Within a short time, she will walk with a stiff gait and may even wobble or appear disoriented. Eventually the animal may be unable to walk and exhibit extreme leg rigidity. Body temperature may increase to over 105° F and respiration rates will increase. At this point death can occur if no treatment is given.

Treatment of eclampsia
If you suspect eclampsia, seek veterinary attention at once and prevent the puppies or kittens from nursing for at least 24 hours. Supplement them with a commercial milk replacer. A veterinarian can confirm eclampsia with a blood test to determine blood calcium levels. Eclampsia can be rapidly corrected by your veterinarian through the use of intravenous calcium supplementation. The bitch or queen is monitored carefully for heart rhythm irregularities which can occur. She will be continued on oral calcium supplements as needed.

If she responds well to treatment, her young can gradually be allowed to nurse.

Prevention of eclampsia
Inappropriate calcium supplementation can predispose a bitch or queen to develop eclampsia. Once a female has had milk fever during a lactation period, there is an excellent chance that it will repeat with future litters if preventative steps are not taken. Supplementation of dietary calcium does not seem to play a large role in preventing eclampsia. In fact, over-supplementation during pregnancy may actually cause it. All calcium supplements must be in the proper ratio with phosphorus. This ratio should be about 1:1 (i.e., 1 part calcium to 1 part phosphorus). In addition, it has been suggested that dog foods high in soybeans will be high in the plant product phytate. Phytates combine with calcium and can render the calcium unavailable to the bitch’s body and therefore make her more susceptible to eclampsia. To remedy the problem, feed diets low in soybean.

In conclusion, it is of great importance for breeders to be able to recognize the signs of eclampsia. If you feel your female is showing these signs, remove the kittens or pups to prevent further nursing and seek veterinary assistance at once.

What is Lymphangiectasia?

As part of the normal circulatory system, lymph fluid is collected from tissues throughout the body and returned to the blood by way of the lymphatic vessels. In intestinal lymphangiectasia, normal drainage is blocked so that intestinal lymph leaks into the intestines instead of being returned to the circulation. This results in the loss of proteins, lymphocytes ( a type of white blood cell), and lipids or fats into the stool.

Intestinal lymphangiectasia may be congenital (present from birth) due to malformation of the lymphatic system, or it may be acquired in association with another disease.

What does intestinal lymphangiectasia mean to your dog & you?

Signs of intestinal lymphangiectasia usually develop slowly over several months, and may come and go. Your dog may fail to gain weight or may progressively lose weight. The loss of protein into the bowel causes loss of fluid from the circulation into the limbs, the abdomen, or the chest. Your dog's legs and/or abdomen may appear swollen and he/she may have trouble breathing. There may be a chronic persistent or intermittent diarrhea due to the loss of protein, fluid and fat into the bowel.

How is intestinal lymphangiectasia diagnosed?

If your dog has the signs described above, your veterinarian will likely suspect one of the diseases that result in loss of proteins into the gut. Laboratory tests and an intestinal biopsy are necessary to diagnose the specific cause.

For the veterinarian:

CLINICAL: diarrhea is usually mild or inapparent, in comparison with other protein-losing enteropathies.

LABORATORY: hypoproteinemia with hypocholesteremia, lymphocytopenia, and/or hypoglobulinemia; frequently also see hypocalcemia due to vitamin D and calcium mal-absorption. It is important to assess liver and kidney function to rule out non-enteric causes of hypoproteinemia.

SURGERY: a biopsy is necessary for definitive diagnosis by histologic examination. At surgery, usually see prominent network of milky distended lymphatic channels in the mesentery or on serosal surface.

How is intestinal lymphangiectasia treated?

This condition can not be cured but it can generally be well-managed by you and your veterinarian. Remissions of several months with occasional flare-ups are common.

The major goal of therapy is to reduce the loss of proteins into the intestine, to restore normal protein levels in your dog. This is done through diet, and medication to reduce inflammation in the intestinal wall. An ideal diet for dogs with intestinal lymphangiectasia contains minimal fat, and an ample quantity of high-quality protein. There are commercial prescription diets available which fulfill these requirements, or your veterinarian can give you information to prepare a low-fat diet at home. In either case, you will need to supplement your dog's diet with fat-soluble vitamins, due to the poor absorption of fat that occurs with this condition.

Corticosteroids are given to reduce inflammation, and thereby reduce loss of protein and associated diarrhea. Your veterinarian may also prescribe antibiotics.


Burrows, C.F., Batt, R.M., Sherding, R.G. 1995. Diseases of the small intestine. In S.J. Ettinger and E.C. Feldman (eds.) Textbook of Veterinary Internal Medicine. p. 1224-1225. W.B. Saunders Co., Toronto.
Williams, D.A. 1998 Protein-losing enteropathy Proc. 16th ACVIM Forum pp 419-421
Copyright © 1998 Canine Inherited Disorders Database. All rights reserved.


Hypoglycemia is the medical term for low blood sugar, which is a condition in which there is a drastic, sudden drop in the level of blood sugar in the puppy. In small breed puppies from post-weaning to 4 month of age, the most common form of hypoglycemia is called Transient Juvenile Hypoglycemia: “Transient” because the symptoms can be reversed by eating; "Juvenile" because it is seen in young puppies.

Background on blood sugar:
Glucose is the "simple" sugar that the body uses for "fuel" to run its various functions. Table sugar, or sucrose, is made up of two simple sugars, glucose and fructose, and can be broken down rapidly after eating. All sugars are carbohydrates. Grains are also carbohydrates but are considered "complex" carbohydrates because they have many more components and take longer to be broken down. The body uses glucose as its primary energy source. All the parts of the body except the brain can, if needed, use alternate energy sources--fatty acids, for example, which the body accesses by breaking down fat stores. The brain, however, is completely dependent upon glucose to function. If the glucose in the blood is lower than normal, the brain function is the first to show signs. The liver is responsible for manufacturing glucose and for storing it in a usable form, for release into the blood stream as needed. Muscle tissues store some of the important materials used in this process. Therefore, a serious liver abnormality or insufficient muscle mass may make it difficult for the body to keep its blood sugar properly regulated.

How are small breeds different?
Puppies of very small and toy breeds of dogs have characteristics that make them more prone to the development of Transient Juvenile Hypoglycemia, which is brought on by fasting. Pups of any breed are more likely to develop hypoglycemia than adults, because their skeletal muscle mass and liver size are smaller and brain size, larger, in proportion to the rest of their body. Therefore, there is less glucose being put out into the blood and more being used by the brain, which is dependent upon adequate glucose in order to function. In small and toy breeds, this discrepancy is more pronounced. Even a brief period of fasting in a toy breed puppy can trigger a hypoglycemic "attack. Puppies with Transient Juvenile Hypoglycemia have normal liver size and function, but inadequate glucose precursors or glucose in its stored form (body fat).

What are the symptoms?
Signs of an attack are a weakness, confusion, wobbly gait, frothing or drooling from the mouth - sometimes even a seizure and drain of blood from the head. A check of the gums will show them to be pale, almost a grayish white in color rather than a healthy bright pink. The puppy can go into shock and, if not cared for properly and promptly, may even die.

What causes it?
Episodes of hypoglycemia often occur without warning. A puppy may be stressed by shipping, or because of their tiny size toy puppies cannot eat a lot at one time, and literally run out of fuel quickly, being chilled, or even exhaustion from too much play may cause the body to use up more sugar than is available. For the young pup prone to this condition, even a brief period of fasting in a toy breed puppy can trigger a hypoglycemic "attack". Recurring hypoglycemic attacks in toy puppies can cause brain damage. Puppies should be fed several times a day a high quality diet. Most puppies will outgrow the problem. Some very tiny dogs will continue to have bouts of hypoglycemia through out their life

What is the Treatment?
Feeding recommendations for puppies at risk for hypoglycemia include: frequent (4-5 times a day) feedings of high-carbohydrate, high -protein and/or -fat foods. Feeding soft moist foods may help to prevent a hypoglycemia attack due to the high sugar content. Gatorade mixed with a little honey, Ringers lactate with dextrose or Pedialyte are good products to use if dog is having an attack. These products have electrolytes, which ailing puppies need. Honey and corn syrup can be used also. For pups who have had recurrent or prolonged signs, monitoring the urine for ketones with a "dipstick" made for diabetics is helpful, since a return to "ketone negative status" signals a return to normalcy. If these measures don't correct the problem, a trip to the vet is recommended. Eating food that is readily digested and metabolized will reverse minor signs, but intravenous glucose administration is required for severe cases.

If your puppy is conscious, give him/her a little Karo Syrup, or Honey under its tongue, or rubbed on its gums. You can also mix honey, or corn syrup with pedialite, stir to dissolve, and dribble it into the puppy's mouth. I think that Nutri-Cal also works extremely well in an emergency. I will give my puppy a ‘squeeze of Nutri-Cal’ into their month. The puppy should begin to improve within about ten to fifteen minutes, if not contact your vet as quickly as you can.

(Nutri-Cal is a high calorie dietary supplement in a low volume form. It is a great tasting vitamin paste. You can purchase this tube for under $10.00. I recommend that you have this on hand for all emergencies and especially when you travel with your yorkie.)

Are there other causes of Hypoglycemia in puppies?
There are numerous other causes of hypoglycemia in puppies, but they are much less common. It is important to distinguish between whether the signs of hypoglycemia occur with fasting or just following a meal. Hypoglycemia can also be an inherited condition. If a female has been hypoglycemic, it's likely that she will pass it on to her puppies. Some problems are caused by liver problems, such as a defect involving an abnormal blood vessel shunt (a "detour," of sorts) around the liver, and some are caused by hereditary metabolic defects, hormone defects and deficiencies, and severe bacterial infections. All of these are serious problems that need to be diagnosed as soon as possible.

Vet@Dog Dr. Lucy L. Pinkston, D.V.M. 3-10-03
Drs Foster & Smith 3-10-2003



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